Colonic responses to enteral tube feeding.
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Biomedical subjects
Publications and source records attributed to T E Bowling.
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BACKGROUND: The traditional fluid fast prior to endoscopy is unnecessary. We have previously shown that drinking water prior to endoscopy does not affect either the quality of mucosal views or residual gastric fluid volumes when compared to patients undergoing endoscopy after a standard fast. The present study was designed to establish whether milk, which may delay gastric emptying, could also be drunk prior to endoscopy without adverse effect. METHODS: Forty-eight patients (mean age 48 years, range 20 to 79) undergoing routine upper gastrointestinal endoscopy after overnight fast were randomized to drink 200 ml of either still mineral water or full fat milk. Endoscopy was performed 90 minutes later, when all residual gastric fluid was aspirated via the endoscope. Volume and pH of gastric aspirate were measured and the quality of the mucosal view at endoscopy recorded as poor, adequate, or excellent. RESULTS: No difference was shown between water (n = 27) and milk (n = 21) drinkers in residual gastric volume (mean +/- SEM, water vs milk) (16.0 ml +/- 1.5 vs 18.9 ml +/- 2.9) or pH (2.23 +/- 0.14 vs 2.48 +/- 0.14). Of those patients with poor, adequate, or excellent views, 4 of 4, 11 of 12, and 6 of 32 patients, respectively, were milk drinkers (chi-squared test for trend = 21.7, df = 1, p < 0.001), indicating significantly worse mucosal views in the group drinking milk. CONCLUSION: Drinking water up to 90 minutes prior to endoscopy is safe, but milk should be discouraged because of suboptimal mucosal views.
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BACKGROUND: Collagenous colitis and lymphocytic colitis present with a similar clinical picture. Whether these conditions are separate entities or whether they represent different pathological stages of the same condition is an unresolved issue. PATIENT: This is a case of collagenous colitis following a fulminant course in which a colectomy was necessary. In the operative specimen the thickened collagen plate, which had been present only two weeks preoperatively had been lost and the pathology was of a lymphocytic colitis. Six months postoperatively this patient developed a CREST syndrome and primary biliary cirrhosis. CONCLUSIONS: This case shows the lability of the collagen plate and the common ground between collagenous and lymphocytic colitis, and presents evidence that these two conditions are different manifestations of the same disease. It also describes for the first time an association between collagenous colitis and CREST syndrome and primary biliary cirrhosis.
BACKGROUND AND AIMS: Radiotherapy has been reported to be of benefit in prolonging the survival of patients with cholangiocarcinoma. This study examined whether radiotherapy in addition to endoscopic stenting improved survival. SUBJECTS: 56 patients with obstructive jaundice due to histologically confirmed non-resectable cholangiocarcinoma. METHODS: A retrospective analysis of these patients who were treated either with endoscopic biliary stenting followed by external beam radiotherapy and internal iridium-192 brachytherapy (n = 28) or with stenting alone (control group; n = 28). RESULTS: The two groups were well matched in age, sex, and stricture type. Eighteen patients had a type I stricture (control group: 11; radiotherapy group: 7) at the time of diagnosis and 38 had a type II or III stricture (control group: 17; radiotherapy group: 21). The median (range) overall survival from diagnosis was seven (1-29) and 10 (4-75) months in the control and radiotherapy groups respectively: This difference did not reach statistical significance (p = 0.06), but survival plots indicated a survival advantage in the radiotherapy group in the first nine months after diagnosis. Approximately one third survived longer than one year in both groups. More patients in the radiotherapy group required a stent change (1.9 v 0.9: p = 0.05), and also had a longer overall inpatient stay (42 days v 19: p < 0.001). When examined on the basis of stricture type, there was a survival advantage in the first 10 months after diagnosis in those with a type II/III stricture (seven and 11 months in the radiotherapy and control groups respectively: 0.01 < p < 0.05). There was no difference in survival between the groups in those with a type I stricture. Numbers surviving longer than one year, stent survival, and number of stent changes were all similar between the two groups when examined on the basis of stricture type, but length of hospital stay remained considerably longer in all patients receiving radiotherapy. CONCLUSION: The survival advantage of radiotherapy in those with a type II/III stricture is seen only in the first 10 months after diagnosis. The costs of radiotherapy and significantly increased time spent in hospital, however, raise doubts over its routine use in the management of non-resectable cholangiocarcinoma.
The development of in-patient malnutrition often begins long before hospital admission. The aim of this retrospective study was to assess the time period taken from when patients first present to their General Practitioners to surgery. Patients undergoing elective intraabdominal surgery over a 3 month period in a district general hospital were divided into two groups: One for those with underlying gastrointestinal malignancy requiring resection (n = 27), and the other in those with chronic biliary disease requiring laparoscopic cholecystectomy (n = 24). Patients with malignant disease presented to the GP at a mean of 3.0 months (SD 2.4) after symptom onset, and those with biliary disease at 3.5 months (SD 2.6). Those with malignancy were then referred and seen by the hospital within a mean of 2.8 weeks (SD 1.3), investigated in 3.3 weeks (SD 2.3) and operated on within 2.7 weeks (SD 1.2). The group with biliary disease were seen in hospital at 6.2 weeks (SD 1.9), investigated in 7.5 weeks (5.8) and operated on at 7.6 weeks (SD 2.1). Overall, the length of time it took from symptom onset to surgery in those with malignant disease was 26 weeks (SD 19), and in those with biliary disease 65 weeks (SD 35). This time period will inevitably lead many patients to become malnourished prior to admission, and this may have implications on the incidence of complications and length of in-patient stay.
So to summarize the key points: 1. concomitant antibiotic therapy, infected diets and possibly hypoalbuminaemia can lead to enteral-feeding-related diarrhoea; 2. the small intestinal responses to both intragastric and intraduodenal enteral feeding are normal and predictable; 3. there is an ascending colonic secretion during enteral feeding which is more profound during intragastric feeding; 4. the suppression of distal colonic motor activity occurs only during high-load feeding and is probably a secondary phenomenon to the hormonal and secretory responses; 5. peptide YY appears to be intrinsically bound up with the causation of the secretory effect; 6. the secretory effect is abolished by intracaecal SCFA.
Since the early 1970s there has been considerable debate over the role of nutritional support in the treatment of patients with acute inflammatory bowel disease. The role of enteral feeding as a primary therapeutic option in patients with acute Crohn's disease remains controversial. This article reviews the role of nutritional support both as an adjunct to standard medical therapy and as a primary therapeutic option.
OBJECTIVE: To describe the case of a women with cholestatic jaundice induced by the spontaneous fragmentation of an oestrogen implant. PATIENT: A 48-year-old woman, who presented with jaundice, pruritus and a flu-like illness 2 weeks after the insertion of a 100 mg oestradiol implant into her right buttock. INTERVENTIONS: At presentation the implant was removed and found to be fragmented. Investigations revealed an oestradiol level of 1548 pmol/l and an oestrogen-induced cholestatic jaundice. RESULTS: After removal of the implant and progesterone therapy, the patients symptoms resolved. CONCLUSION: This is the first reported case of cholestatic jaundice induced by a subcutaneous oestrogen implant.
In summary, POI is a predictable event with actual return of bowel function preceding clinically detectable signs of function by at least 24 h. All parts of the gastrointestinal tract are affected, but small-intestinal function returns first, probably as early as 4-8 h after surgery in many cases. The timing of restarting feeding could be earlier than current practice would suggest, and because of the more rapid recovery of small-intestinal function it could be argued that post-pyloric feeding, at least in the first 24-48 h, may be preferable. While a policy of refeeding only when bowel function is clinically detectable is acceptable for many patients, there are certainly some who would benefit from feeding at an earlier stage. Parenteral feeding is expensive and a greater knowledge of the mechanisms underlying POI may lead clinicians to different and perhaps more appropriate methods of management.
Diarrhoea complicating enteral feeding is a common clinical problem affecting up to 25% of patients. Its pathogenesis remains unknown. A new technique of human in vivo segmental colonic perfusion was used to investigate colonic water and electrolyte movement in response to enteral feeding. Four groups of studies were performed in which low and high load polymeric enteral diet infusions were undertaken, either intragastrically or intraduodenally (n = 6 each group). Net absorption of sodium, chloride, and water occurred during fasting throughout the colon in all groups. There was a significant net secretion of sodium, chloride, and water in the ascending colon during low load (sodium: -42 mmol/h; 95% confidence limits -52 to -19, Chloride: -18 mmol/h; -50 to +16, water: -174 ml/h; -348 to -30) and high load (sodium: -24 mmol/h; -60 to +8, chloride: -18 mmol/h; -31 to +16, water: -120 ml/h; -246 to +6) gastric feeding, and during high load duodenal feeding (sodium: -12 mmol/h; -22 to -6, chloride; -6 mmol/h; -16 to +3, water: -72 ml/h; -144 to -6). Net secretion persisted in the distal colon only during high load gastric feeding. In the other three groups there was a net absorption in the distal colon. This study identified a significant colonic secretory response to enteral feeding, which is related to the site and load of the diet infusion. This response may play an important part in the pathogenesis of enteral feeding related diarrhoea.
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Diarrhoea complicates enteral feeding in up to 25% of patients. In-vivo perfusion studies in healthy subjects have shown secretion of salt and water in the ascending colon in response to enteral feeding. This study investigated the effect of short-chain fatty acids (SCFA) on this secretory response. Six healthy volunteers underwent segmental in-vivo colonic perfusion. First, baseline fasting colonic water and electrolyte movement was established, then a standard polymeric enteral diet was infused into the stomach while the colon was perfused with either a control electrolyte solution or a test solution containing SCFA. The electrolyte concentrations and osmolality of the two perfusates were identical. In the fasting state water was absorbed throughout the colon. During the control infusion there was significant (p < 0.05) secretion of water in the ascending colon (median rate 1.0 mL per min [95% CI 2.8 mL per min secretion to 0.8 mL per min absorption]). During the SCFA infusion the secretion was significantly reversed (p < 0.05) and there was net absorption (1.6 [0.8-3.7] mL per min). In the distal colon water absorption was significantly greater during the control infusion than during fasting (3.7 [2.5-4.6] vs 1.3 [0.3-2.2] mL per min); during the test infusion this absorption persisted (2.8 [1.3-3.6] mL per min). Movement of sodium, chloride, and potassium ions was similar to that of water in all stages of the study. Bicarbonate movement did not significantly change at any stage. Infusion of SCFA directly into the caecum reverses the fluid secretion seen in the ascending colon during enteral feeding. This finding could have implications for the management of diarrhoea related to enteral feeding.
To investigate the effects of supplemental oxygen on cardiac rhythm during gastroscopy, 103 patients aged over 60 were randomised to receive either supplemental oxygen or air at 2 litres/minute during the procedure. Pulse rate, blood pressure, oxygen saturation, and a Holter cardiac trace were monitored before, during, and for one hour after the gastroscopy. A wide range of electrocardiographic abnormalities were recorded in both oxygen and air groups, of which ventricular and supraventricular ectopic beats were the most common. There were no significant differences in the rate of occurrence of any clinically important cardiac abnormality either between the oxygen and air groups or between the three monitored periods before, during, and after gastroscopy. There were significantly fewer patients, however, with supraventricular extra systoles when oxygen was given during gastroscopy (p < 0.05). Although supplemental oxygen during gastroscopy significantly improved oxygen saturation (p < 0.001; 95% confidence intervals for the difference between the means: 2.9 to 4.7), there was no correlation between oxygen saturation and any electrocardiographic changes. It is concluded that electrocardiographic abnormalities are common in patients over 60, but this study found no evidence that they are induced by gastroscopy. Supplemental oxygen increases oxygen saturation but does not reduce the incidence of clinically important cardiac arrhythmias.
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